Preservation of cerebral cortical function following transient arteriovascular ischemia requires an understanding of sequelae attendant upon cerebrovascular stroke. We have developed a primate (monkey) animal model of unilateral, arteriovascular stroke of predetermined duration and subsequent arteriovascular reperfusion. Utilizing this cerebrovascular stroke model combined with controlled perfusion of exposed cerebral cortices, we can investigate the status of the functional patency of cerebromicrovasculature during post ischemic reflow. Moreover, we can directly can insight into the pathophysiology of cerebral cortical edema following transient ischemia of cerebral cortex. Cerebral cortical edema and decreased vascular reperfusion following transient cerebrocortical ischemia may propagate, prolong and enhance the initial ischemic injury and compromise neuronal elements surviving but only marginally so the initial transient insult. The primate animal model outlined permits detailed investigation of these secondary factors and permits contrast of findings (in the same animal) following unilateral, hemispheric cerebrovascular stroke with similar parameters determined for the contralateral control hemisphere.